THURSDAY, May 25, 2006 (HealthDay News) -- Patients got some relief from the disfiguring disease scleroderma after taking a statin, a drug widely used to lower blood cholesterol, Japanese researchers report.
Doctors tried the drugs after speculating that the condition may be caused by defective vasculogenesis -- the process of forming new blood vessels, according to a report in the May 25 issue of Arthritis & Rheumatism by physicians at the Keio University School of Medicine in Tokyo.
"In many ways, this makes perfect sense," said Kirkwood Pritchard, vice chairman of research for surgery at the Medical College of Wisconsin, who conducts research on scleroderma and other conditions affecting blood vessels. "Statins have many beneficial effects on blood vessels," he said.
Scleroderma is believed to be an autoimmune disease in which the body's tissues produce too much collagen, forming thick connective tissue that builds up around the cells of the skin and internal organs. The mildest form of the disease causes thick, reddish patches of skin, most often on the chest, stomach or back. More severe forms can attack internal organs.
An estimated 30,000 Americans suffer from scleroderma, and about 10,000 people die each year from systemic sclerosis, the most severe form of the condition, according to the Scleroderma Foundation.
The root cause of scleroderma is unknown, but the disease is known to affect primarily small arteries and decrease blood flow to the extremities.
The Japanese study was intended to determine whether and how much blood flow could be improved and scleroderma symptoms relieved by one of the most popular statins, Lipitor.
Fourteen women who had systemic sclerosis, some for more than 20 years, took 10 milligrams of Lipitor daily for 12 weeks. Their symptoms were evaluated during the treatment period and then four weeks later. Most significantly, they also were tested for blood levels of circulating endothelial precursors (CEPs), molecules essential for the formation of blood vessels.
CEP levels did increase anywhere from 1.7-fold to eightfold for those women who completed the study. But for 8 participants, CEP levels peaked either at weeks 4 or week 8 of the trial, then decreased gradually. And in the five women whose CEP levels increased throughout the study, those levels fell short of those seen in healthy individuals. Symptoms declined during the study, but then returned to their old levels after the drug was discontinued.
Scleroderma is "an extreme example of oxidate stress and inflammation" that damages blood vessels, and "statins are known to improve vascular health in a lot of ways," Pritchard said. Among other actions, they help prevent blood vessels from acting as they should, he said.
Statins themselves might not be the answer to scleroderma, but the approach of using experimental drugs to protect blood vessels and promote the growth of new ones looks highly promising, Pritchard said.
A statement by Dr. Masataka Kuwana, who led the Japanese study, acknowledged that these findings were just a first step.
"Further multi-center, placebo-controlled trials involving a large number of systemic sclerosis patients are necessary to confirm the clinical benefits of statins," Kuwana said.
More information
To learn more, visit the Scleroderma Foundation.
